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Smoking causes a dose-dependent increase in granulocyte-bound L-selectin
Shalini Patiar1, Dominic Slade, Ursula Kirkpatrick
1Academic Surgery Unit, South Manchester University Hospital, Southmoor Road, Wythenshawe, M23 9LT, Manchester, UK.
Thrombosis Research
|August 8, 2002
Summary
Cigarette smoking acutely increases granulocyte L-selectin expression, a key factor in cell adhesion and atherosclerosis development. Smokers with peripheral vascular disease had lower serum L-selectin, suggesting increased consumption.
Area of Science:
- Cardiovascular Research
- Immunology
- Vascular Biology
Background:
- Atherosclerosis development is linked to cigarette smoking, involving endothelium and leukocytes.
- The precise mechanism remains unclear, prompting investigation into acute effects.
Purpose of the Study:
- To investigate the acute effects of cigarette smoking on granulocyte L-selectin expression and serum L- and E-selectin levels.
- To compare these effects in healthy controls and patients with peripheral vascular disease (claudicants).
Main Methods:
- Flow cytometry was used to measure granulocyte L-selectin expression (mean fluorescence intensity).
- Enzyme-linked immunosorbent assay (ELISA) quantified serum L- and E-selectin levels.
- Measurements were taken before and after smoking in 12 claudicants and 12 healthy controls.
Main Results:
- Granulocyte L-selectin expression increased dose-dependently after smoking in both groups (p<0.002 and p<0.001).
- Serum L-selectin was significantly lower in claudicants compared to controls (p<0.005).
- Serum E-selectin and L-selectin levels did not change post-smoking.
Conclusions:
- Acute smoking increases granulocyte L-selectin, potentially promoting granulocyte-endothelial adhesion and contributing to atherosclerosis.
- Lower baseline serum L-selectin in claudicants and lack of increase post-smoking suggest consumption via activated endothelial receptors, possibly a negative feedback mechanism.